An arrhythmia, as used herein, is described as a disturbance in the normal rate, rhythm or conduction of the heartbeat. More specifically, an atrial arrhythmia is such an arrhythmia which has its site of origin in the atria. An atrial tachycardia is a condition where the atria contract at a high rate, e.g., 100 or more beats per minutes. In paroxysmal (temporary) atrial tachycardia (PAT) an ectopic atrial focus becomes a pacemaker for the heart for the duration of the tachycardia. This duration may vary from seconds to several days. The irritable atrial focus that causes the atrial tachycardia normally causes ventricular tachycardia at the same frequency when AV conduction is normal. Another arrhythmia is termed "atrial flutter," in which situation a re-entry circuit in the atrial wall is the pacemaker of the heart, stimulating it with a frequency of approximately 200 to 300 beats per minute. In this situation, the AV node normally blocks every second, third or fourth impulse from the atrium and the ventricular frequency therefore varies from 60 to 50 bpm; the ventricular rate is regular when the block is constant, but irregular when the block varies.
In atrial fibrillation (AF), there is a chaotic and turbulent activation of atrial wall tissue. The number of depolarizations per minute exceeds 400 and the stimuli occur in the refractory period of the surrounding atrial myocardium. Under these conditions, the depolarization of the atrial wall is not coordinated, and a chaotic and non-effective activity controls the heart. With this irregular atrial activity, the AV node does not conduct every atrial stimulus, and the ventricles receive impulses in an irregular fashion.
Another form of atrial arrhythmia is the premature atrial contraction (PAC) or atrial extrasystole. The PAC is basically an atrial contraction which arrives early, before it is expected. While the sinus node is normally the pacemaker of the heart, when a PAC occurs a focus takes over the function of the sinus node for one beat. After such an ectopic atrial beat, the next beat from the sinus node is slightly delayed. Thus, the PAC causes an irregular cardiac rhythm. The irregularity may, in certain situations, be regular, as in Bigeminy or Trigeminy, i.e., one or two normal beats between each PAC. PACs may be a prelude to atrial tachycardia. As is known, tachyarrhythmias pose a danger of fibrillation, which in turn can be life threatening. Tachyarrhythmias are also associated with other low cardiac output symptoms, such as fatigue and syncope, and other undesirable manifestations. While many supra-ventricular tachyarrhythmias (SVT) are episodic, and marked by abrupt onset but also abrupt termination, they cause considerable patient distress and, if untreated, can lead to dangerous life-threatening conditions. The major danger of supra-ventricular tachyarrhythmias, especially chronic atrial fibrillation, is the development of blood clots which can cause stroke and possibly death.
In the patient where atrial tachycardia is the result of ectopic atrial focus in the pacemaker, one method of treatment is ablation the heart tissue where the focus is to be found. However, this is an expensive and dangerous procedure. Other techniques include anti-tachycardia, or cardioversion-type stimulation, where either a train of high rate pulses or one or more high energy pulses is delivered to the patient's heart in an attempt to restore a more normal rhythm. While these techniques can be valuable, and have achieved some success rate, it is clearly more desirable to treat a patient with an incipient atrial problem, to suppress it or to otherwise prevent the dangerous atrial arrhythmia from occurring in the first instance. Thus, it is known that incidences of PACs, if not treated, can develop into a more dangerous atrial arrhythmia, including tachycardia or fibrillation.
Another potential cause of atrial arrhythmia is ischemia, which is brought on due to restricted blood circulation to the cardiac tissue. When one performs exercise, the body can build up an oxygen debt or oxygen depletion. Under normal post-exercise circumstances, for a heathy patient, the cardiac rate remains high for a period of time, which ensures a sufficient blood flow to the heart. However, if the post-exercise rate drops too fast, this can result in ischemia. While the effect depends on the level of exercise and the duration of the exercise, for patients at risk of atrial tachycardia or fibrillation, there is a need to ensure that the cardiac rate does not decrease too rapidly after exercise episodes.
What is needed in the pacing art is a new therapy approach to provide pacing treatments which anticipate the causes of such dangerous atrial arrhythmias and which respond when needed to suppress the onset of such an arrhythmia. For example, there is a need for a pacing therapy designed to condition a patient's heart so as to provide stable consistent conduction pathways and refractory periods in the atrium, which can be achieved by stimulating the atrium from the same site and at stabilized rates. Similarly, the incidence of PACs can be reduced by increasing the heart rate when appropriate, e.g., by increasing the pacing rate to a stabilized higher rate following the occurrence of a PAC. Also, cardiac refractory dispersion can be reduced by providing a smooth transition from the PAC coupling interval to the underlying heart rate. Further, following patient exercise, the danger of ischemia and refractory dispersion can be reduced by taking over with pacing and limiting the decrease of pacing rate so that a higher than intrinsic rate is maintained for some period of time, thus providing a higher delivery of oxygen to the heart post-exercise.